Skin Microbiome Medicine for Dermatology - Dermatology Advisor

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Breakthroughs in Skin Microbiome Medicine May Transform Dermatology

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Bryant Furlow

February 23, 2026

Human skin harbors complex microbial communities of bacteria, viruses, and fungi. A growing body of research shows that shifts in the species composition, diversity, and metabolic products of the skin ecosystem can open the door to invasion by harmful microbes, inflammatory responses, skin barrier dysfunction, and dermatologic disease.

"We have a complex relationship with our skin microbes, which are integral to immune homeostasis and repair, as well as mediators of local and systemic inflammation," explained Nathan Archer, PhD, assistant professor of dermatology at Johns Hopkins University School of Medicine.

The clinical implications of utilizing the skin microbiome in the treatment of dermatologic diseases could be profound.

Shifts in microbial community structure — especially reduced overall species diversity and the resulting predominance of pathogenic and pro-inflammatory species — precede the onset or worsening of symptoms in atopic dermatitis, eczema, acne, and psoriasis.^1-5 Large-scale genomic sequencing has identified previously unsuspected bacterial communities and microbial signatures that can help distinguish lesional skin from healthy skin, pointing toward new diagnostic and therapeutic targets.^1,5-7

Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair.

Recent research has also demonstrated that disruptions of skin ecology, called dysbiosis, are more consistently associated with acne and other inflammatory dermatoses than the overgrowth of Cutibacterium acnes or Staphylococcus aureus. Dysbiosis contributes directly to disease flares, challenging longstanding assumptions about the etiology of dermatologic diseases.^4,8,9 Indeed, dysbiosis appears to be a hallmark mechanism in inflammatory dermatoses like eczema, rosacea, and psoriasis, driven by altered microbiome-immune system interactions.⁸

Scientists are exploring how ecological engineering of the skin microbiome might offer alternatives to current therapies like antibiotics, which eradicate both pathogens and beneficial microbes and may worsen dysbiosis and induce treatment resistance.^10,11

"Understanding their roles opens the door to entirely new therapeutic paradigms: instead of only suppressing inflammation, we can begin to restore balance between our skin and the microbial community," Dr Archer said.

For example, preclinical research suggests that applying commensal bacteria can improve the integrity of the skin barrier and reduce S aureus overgrowth in atopic dermatitis.^10,12 Researchers are also investigating prebiotics, strain-specific probiotics, live bacteriotherapies, genetically engineered bacteriophages, and targeted phage cocktails for selectively culling pathogens from skin ecosystems.^7,10,11,13    

The field of microbiome dermatology is young and not without significant challenges, including the need for better standardization of research methodologies and further expansion of research ventures.^4,5 Yet experts maintain optimism about knowledge gained thus far and that these challenges will be overcome. They anticipate a clinical paradigm shift toward precision microbiome medicine in the years ahead.

The Skin Microbiome Beyond the Skin

The skin's microbial ecosystem includes a dermal microbiome beneath the skin's surface and a distinct epidermal microbiome interfacing the external environment, shaped by infants' early encounters with microbes, explained Richard Gallo, MD, PhD, professor and chair of the department of dermatology at the University of California San Diego School of Medicine. Intriguingly, Dr Gallo and his colleagues found that these microbial communities communicate with the microbiomes of other organ systems, like the gut.^14,15

Skin wounds affect intestinal bacteria, for example.¹⁶ "Our work discovered that injury or inflammation of the skin causes release of 'danger signals' that are detected by cells in the intestine," Dr Gallo said. "These cells then respond by producing antimicrobials that inappropriately kill some of the bacteria in the gut that help maintain gut health. This is important as it provides an explanation for the frequent co-occurrence of diseases of the skin and gut, and emphasizes the need to treat the whole patient, not just a single organ."

This skin-to-gut axis is not the only connection between skin and other microbiomes, Dr Gallo was quick to point out. "Important communication occurs between skin and lung, skin and brain, and skin and the cardiovascular system," he explained. "With continued work, we see important general medical breakthroughs coming from understanding these communication networks."

Indeed, a recent study showed that S aureus skin exposure can exacerbate lung inflammation, helping to explain the atopic march from atopic dermatitis to respiratory disease.¹⁷

"Clinically, this highlights the importance of early intervention in atopic dermatitis — addressing microbial dysbiosis and interleukin (IL)-36-driven inflammation before diseases of the atopic march develop, such as asthma," said Dr Archer.

For patients with overlapping atopic dermatitis and neutrophilic asthma, that finding bolsters the case for a more integrated clinical approach to achieve better outcomes, Dr Archer added. "Rather than treating skin and airway disease in isolation, clinicians might consider shared immunological pathways as therapeutic targets or agents that modulate or restore healthy microbial balance that could, in principle, benefit both skin and lung inflammation," he said.

Biomarkers like IL-36 and neutrophil signatures might be helpful for risk assessment and early therapeutic escalation in patients with atopic dermatitis, to prevent neutrophilic asthma progression, Dr Archer added.

"Elevated systemic IL-36 and neutrophil signatures could identify patients whose atopic dermatitis may be leading towards neutrophilic asthma or T2-low asthma, which is more treatment-resistant than T2-high asthma," he explained. "In fact, circulating IL-36 has already been associated with severe asthma in patients."

With his coauthors, Dr Archer also reported that bacteria like S aureus can promote skin regeneration through IL-1β-dependent signaling pathways, with important implications for wound care.¹⁸

"This suggests that indiscriminate topical antibiotic use may disrupt beneficial microbe-host interactions that aid healing," Dr Archer explained. "Microbiome-aware wound care that balances pathogen control with preservation of beneficial microbes may improve regenerative outcomes."

Atopic dermatitis and asthma are heterogeneous conditions with immunological subtypes, Dr Archer pointed out, and better understanding of their mechanistic underpinnings will enable the development of more personalized treatment approaches.

"Understanding which cytokine and microbial pathways drive an individual's disease — whether it be IL-36–neutrophil, Th2, or S aureus — may enable personalized therapy selection and better prediction of comorbidities like asthma or food allergy," Dr Archer said. "We are moving away from a one-size-fits-all mentality and entering an era of precision dermatology. Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair."

Are Skin Diseases Industrial Comorbidities?

In addition to genomics and molecular mechanism studies, insights into healthy skin microbiomes are being gleaned from cross-cultural research.

"Over the last few decades we've seen a steady rise in chronic inflammatory skin conditions, especially in Western countries and in places rapidly adopting Western lifestyles," explained study coauthor Julia Durack, PhD, Executive Director of the Holobiont Medical Research Foundation. "These diseases are much less common in traditional, non-industrialized communities. Because the skin microbiome is closely tied to skin health, we wanted to study the Yanomami, one of the last remaining hunter-gatherer groups, who rarely experience these conditions. By looking at their skin microbiome, we hoped to better understand what might be missing in modern populations and how that relates to the rise in skin disorders."

What they found was that the skin of this group who reside in the remote Amazonian rainforest share some bacterial communities with Western-nation populations, but with markedly greater species diversity (R² =.455; P =.001).¹⁹ A total of 115 previously unknown bacterial genomes were identified as part of the skin microbiome of these individuals.

"The Yanomami community we worked with has had very limited contact with outsiders, so it's unlikely that the shared taxa we observed were introduced by westerners. Instead, these are what we would call conserved microbial groups — taxa that are commonly found across humans and even other mammals," Dr Durack said. "What was particularly interesting in our data was that while the Yanomami share some of these same microbial groups with Western populations, the diversity within those groups was much greater. For example, their skin harbored a wider range of Staphylococcus species, including ones we didn't detect at all on Western skin. That suggests their microbiomes are not only intact but also more complex, reflecting a deeper ecological richness rather than acquisition from outside contact."

That wasn't just a reflection of the Yanomami people living in the species-rich tropics, where there are more bacterial and fungal species in general, Dr Durack said.

"People living traditional lifestyles tend to have more species-diverse skin microbiomes, and this is consistent across non-industrialized groups worldwide, not only those in the tropics," she explained. "The key factor appears to be lifestyle rather than geography. In industrialized societies, our skin microbiomes are less diverse and compositionally distinct, shaped by constant exposure to chemicals, pollution, antibiotics, and a lack of contact with beneficial microbes from soil, plants, and other natural environments."

Dr Durack and other researchers refer to conditions like acne, rosacea, psoriasis, and atopic dermatitis as industrialized comorbidities, meaning they are strongly linked to the ecological and microbial shifts that come with modernization and not something inherent to genetics or ancestry, she said.

For example, other researchers found that when urban children in Finland have more natural play areas, their skin microbiome's species diversity grows within a few weeks, along with measurable changes in immune regulation markers.²⁰

"This suggests that reintroducing environmental microbial exposures can directly influence health," Dr Durack said. "Our study extends this idea by showing that the Yanomami's continuous exposure to diverse environmental microbes likely helps maintain a complex skin microbiome. That complexity may be protective and its loss in industrialized societies could help explain the rise in inflammatory skin conditions we now consider hallmarks of modern living. Restoring microbial diversity on the skin could be an important way to boost resilience against inflammatory conditions."

The skin microbiome of a westernized adult who temporarily lived with the Yanomami shifted to Yanomami-like microbiomes, Dr Durack said, though it was lost upon their return to an industrialized setting.¹⁹

"That tells us it's not a closed door. Our skin microbiomes can adapt," she said. "In industrialized societies, we've largely lost this co-evolved relationship with our environment. While it may not be realistic to completely rewild our skin microbiomes to an ancestral state, Western medicine could take a more ecological approach: finding ways to reintroduce or support the right kinds of microbial exposures that strengthen the skin barrier and immune balance. This could open new avenues for preventive and therapeutic strategies in dermatology."

Challenges and Furthering the Research

Not surprisingly for an emerging field of knowledge, researchers caution that mechanistic uncertainties and gaps in methodological standardization must be addressed to strengthen preclinical research, and that large, well-designed, standardized clinical studies are needed to more clearly establish causality between the microbiomes and disease.^21,22

Early work with targeted bacteriophage culling has been promising so far, but little is yet known about long-term effects on commensal species, the potential for evolved resistance to phages, or off-target effects on beneficial microbes.¹³

Nor do we yet know the best strategies for ecological engraftment (defined as sustained integration of introduced species into the skin microbiome) or how species diversity and composition might affect resistance to introduced species.⁷

Yet direct-to-consumer marketing hype has gotten well ahead of the science, Dr Gallo cautioned. "An unfortunate lack of scientific rigor has occurred that has led to false claims and unrealistic expectations," he said. "The field is working through this, but several products are still sold without good scientific evidence that they are effective."

The field has taken its first tentative steps, but has yet to find its stride. "We still need to define how specific microbes and their products shape skin and systemic immunity, and when dysbiosis becomes pathologic," Dr Archer said. "This includes microbe-neuro-immune interactions, which are only beginning to be uncovered in the skin with much to be discovered about how skin microbes may affect distal neural development."

We also don't yet understand what nutrients skin microbes use, or how exactly transitions between homeostatic and inflammatory states might cause metabolic shifts in the microbiome, he noted.

"Longitudinal, mechanistic, and multi-tissue studies will be essential to close these gaps," Dr Archer said. "We are currently investigating how pathogenic bacteria gain a foothold onto our skin and why certain pathogens are commonly prevalent among multiple inflammatory skin conditions.If we can understand the strategies by pathogens to live on our skin, we hope to prevent colonization and exacerbation of inflammatory skin disorders that involve dysbiosis."

"We're only just beginning to understand how important the skin microbiome is for our overall health," agreed Dr Durack. "Most of what we know so far is based on studies of people in industrialized societies, which gives us a very narrow view. By broadening research to include communities with diverse ethnicities, lifestyles, and environments, we can uncover much more relevant insights into what truly supports healthy skin — and how modern lifestyles may be limiting that potential."

Disclosure: Weiss Biosciences Inc. funded the Yanomami skin microbiome study and paid Dr Durack's salary. Dr Nathan Archer has received previous grant support from Pfizer and Boehringer Ingelheim and was a paid consultant for Janssen Pharmaceuticals and Alphyn Biologics. Dr Gallo had no relevant disclosures.

References:

1. Chaudhary PP, Myles IA, Zeldin J, et al. Shotgun metagenomic sequencing on skin microbiome indicates dysbiosis exists prior to the onset of atopic dermatitis. Allergy. 2024;78(10):2724-2731. doi:10.1111/all.15806
2. Kim HB, Alexander H, Um JY, et al. Skin microbiome dynamics in atopic dermatitis: understanding host-microbiome interactions. Allergy Asthma Immunol Res. 2025;17(2):165-180. doi:10.4168/aair.2025.17.2.165
3. Asees A, Sadur A, Choudhary S. The skin microbiome in rosacea: mechanisms, gut-skin interactions, and therapeutic implications. Cutis. 2025;116(1):20-23. doi:10.12788/cutis/1240
4. Niedzwiedzka A, Micallef MP, Biazzo M, Podrini C. The role of the skin microbiome in acne: challenges and therapeutic opportunities. Int J Mol Sci. 2024;25(21):11422. doi:10.3390/ijms.252111422
5. Ruuskanen MO, Vats D, Potbhare R, et al. Towards standardized and reproducible research in skin microbiomes. Environ Microbiol. 2022;24(9):3840-3860. doi:10.1111/1462-2920.15945
6. Li Chengchen, Ravikrishnan A, Wijaya I, et al. Large-scale skin metagenomics reveals extensive prevalence, coordination, and functional adaptation of skin microbiome dermotypes across body sites. bioRxiv. Published online ahead of print June 8, 2025. doi:10.1101/2025.04.24.650393
7. Oh J, Voigt AY. The human skin microbiome: from metagenomes to therapeutics. Nat Rev Microbiol. Published online August 4, 2025. doi:10.1038/s41579-025-01211-9
8. Wilkhoo HS, Islam AW, Hussain S, Kadam SR, Rao ZK, Singh B. Skin microbiome and inflammatory dermatoses: a focused review. Costmoderma. 2025;5:107. doi:10.25259/CSDM_99_2025
9. Huang C, Zhuo F, Han B, et al. The updates and implications of cutaneous microbiota in acne. Cell Biosci. 2023;13:113. doi:10.1186/s13578-023-01072-w
10. Lyu Y, Shen J, Che Y, Dai L. Skin microbiome engineering: challenges and opportunities in skin disease treatment. iMetaOmics. 2025;2:e70012. doi:10.1002/imo2.70012
11. Ito Y, Amagai M. Controlling skin microbiome as a new bacteriotherapy for inflammatory skin diseases. Inflamm Regen. 2022;42:26. doi:10.1186/s41232-022-00212-y
12. Uberoi A, Murga-Garrido SM, Bhanap P, et al. Commensal-derived tryptophan metabolites fortify the skin barrier: insights from a 50-species gnotobiotic model of human skin microbiome. Cell Chem Biol. 2025;32(1):P111-P125.E6. doi:10.1016/j.chembiol.2024.12.007
13. Natarelli N, Gahoonia N, Sivamani RK. Bacteriophages and the microbiome in dermatology: the role of the phageome and a potential therapeutic strategy. Int J Mol Sci. 2023;24(3):2695. doi:10.3390/ijms24032695
14. Nakatsuji T, Chiang H, Jiang SB, Nagarajan H, Zengler K, Gallo RL. The microbiome extends to subepidermal compartments of normal skin. Nat Commun. 2013;4:1431. doi:10.1038/ncomms2441
15. Nakatsuji T, Cheng JY, Gallo RL. Mechanisms for control of skin immune function by the microbiome. Curr Opin Immunol. 2021;72:324-330. doi:10.1016/j.coi.2021.09.001
16. Dokoshi T, Chen Y, Cavagnero KJ, et al. Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice. Nat Commun. 2024;15:3009. doi:10.1038/s41467-024-47072-3
17. Kline SN, Feller LE, Saito Y, et al. Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march. Cell Reports. 2025;44(8):116054. doi:10.1016/j.celrep.2025.116054
18. Wang G, Sweren E, Liu H, et al. Bacteria induce skin regeneration via IL-1β signaling. Cell Host Microbe. 2021;29(5):777-791.e6. doi:10.1016/j.chom.2021.03.003
19. Durack J, Piceno Y, Vuong H, et al. Yanomami skin microbiome complexity challenges prevailing concepts of healthy skin. Nat Comm. 2025;16:5542. doi:10.1038/s41467-025-60131-7
20. Roslund MI, Puhakka R, Grönroos M, et al. Biodiversity intervention enhances immune regulation and health-associated commensal microbiota among daycare children. Sci Adv. 2020;6(42):eaba2578. doi:10.1126/sciadv.aba2578.
21. Metwaly A, Kriaa A, Hassani Z, et al. A consensus statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research. Nat Rev Gastroenterol Hepatol. 2025;22:343-356. doi:10.1038/s41575-025-01041-3
22. Shahid U. Microbiome-guided precision medicine: mechanistic insights, multi-omics integration, and translational horizons. J Precis Med: Health Dis. 2025;3:100018. doi:10.1016/j.premed.2025.100018

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Trending Sun Protection Myths: Addressing Misinformation in Clinical Practice

12–15 minutes

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For most, sunscreen is considered the foundation of basic skin care. Yet years of hard-won progress in embracing sun safety among the public has taken a hit from recent misinformation spreading online about sun protection practices.

A 2025 study found an abundance of TikTok videos with the hashtag #nosunscreen that support many of the growing myths about sun protection, including the belief that sunscreen use is not important or may even be harmful to one's health.¹ This misinformation is quickly gaining traction, as Nikookam and colleagues reported that the #nosunscreen hashtag had surpassed 11.7 million views on TikTok while the #AntiSunscreen hashtag had garnered more than 5.3 million views at the time of their writing. These authors also reported a surge in Google searches for anti-sunscreen content.²

Dermatologist Perspectives on Sun Protection Myths

The myriad of myths regarding this topic have increasingly made their way into the dermatologist's office, with physicians reporting a growing number of patients espousing these inaccurate views.

"We are encountering an alarming rise in myths regarding sunscreen and sun protection," said Annie Grossberg, MD, associate professor of dermatology and director of pediatric dermatology at Johns Hopkins Medicine in Baltimore, Maryland.^1-3 "Some of these include misinformation about the dangers of sunscreen and the necessity of wearing sunscreen."

[T]he benefits of sunscreen in preventing melanoma and other skin cancers far outweigh theoretical risks in studies that have shown no harm of sunscreens in humans. 

Additional myths in this realm include the notions that one can develop a solar callus for sun protection or simply use coconut oil, beef tallow, or other oils in place of sunscreens approved by the United States Food and Drug Administration (US FDA).

"The rise in misinformation is likely multifactorial, but the viral nature of social media is a major contributor," Dr Grossberg said. "Influencers with broad audiences can post anecdotes or opinions and present this as factual and in a sensationalist manner, despite a lack of supporting evidence."

"Algorithm-driven platforms reward sensational natural health narratives, and influencer anecdotes travel faster than peer-reviewed data, while distrust of chemical ingredients dovetail with broader wellness and clean-beauty marketing," added dermatologist Swati Kannan, MD, associate professor of dermatology and Mohs surgeon at the University of California San Diego.

Veena Vanchinathan MD, a dermatologist and member of the American Academy of Dermatology (AAD), says that she most often hears these misconceptions from younger patients and those active on social media platforms. "Patients may ask if natural oils are better, express concerns about chemical sunscreens, or mention tanning as a way to build protection from UV damage," she shared. "These conversations often present an opportunity for me to thoughtfully partner with my patients and share impactful education."

Dr Kannan has also experienced an increase in similar questions in her practice. "Patients increasingly ask if they can swap to coconut oil, voice fears that sunscreen causes cancer, or request guidance on beef tallow recipes circulating on TikTok," she said. "My response to all of this is that we have so much evidence to support the use of sunscreen to prevent skin cancers and melanomas, and we do not have any evidence that sunscreen is carcinogenic or that natural treatments provide enough sun protection."⁴

Dr Grossberg recalls many instances of patients and parents asking about the safety of sunscreens and seeking more natural alternatives. Some parents are genuinely afraid to use sunscreens on their children due the misinformation they have heard about on social media, she explained. 

"These are well-meaning parents who want to do the best and safest things for their children and themselves, but these scenarios reflect how deeply some of this social media-driven misinformation has permeated everyday decision making," Dr Grossberg continued. "The challenge lies in redirecting these concerns towards evidence-based solutions."

6 Common Myths and Truths About Sun Protection

Below are the most common myths that dermatologists may encounter in clinical practice, as well as the accurate, evidence-based take on each point.

"Sunscreen is only necessary at the beach, on vacation, or if it's sunny outside." 

"Sun protection is essential every day, not just on vacations, at the beach, or on the hottest days of the summer," Dr Grossberg advised.⁵ "UV exposure and damage from the sun is cumulative, begins in childhood, and happens during everyday activities."

Additionally, "Up to 80% of UV rays can penetrate clouds, and UVA penetrates glass, so daily use is recommended regardless of the weather," Dr Vanchinathan noted.⁵

"Along with sun protective clothing, sunscreen remains one of the most effective tools we have for prevention of skin cancer and skin aging," Dr Grossberg said.

Both the AAD and the American Cancer Society recommend using a broad-spectrum, water-resistant sunscreen with a minimum of SPF of 30.^6,7

"People with darker skin tones don't need sunscreen."  

"While skin cancer risk may be lower in patients with skin of color, these individuals are still at risk for photoaging, pigmentary disorders, and UV-induced skin cancers," Dr Vanchinathan explained.⁸ "Daily photoprotection helps prevent pigmentary disorders such as melasma and post-inflammatory hyperpigmentation, in addition to skin cancers."

"When we eventually diagnose melanomas in darker-skinned patients, it tends to be later-stage and more aggressive disease," Dr Kannan noted.⁸ "Although melanin provides some natural SPF, it is insufficient against cumulative UV damage, so consistent sunscreen use is still recommended for all skin types."

"Sunscreen is toxic and causes cancer." 

"Approved UV filters have never shown carcinogenicity in humans, whereas UV radiation is a proven human carcinogen," Dr Kannan emphasized.⁹

"Decades of safety data and FDA evaluation support the use of both mineral and chemical sunscreens as safe and effective when used as directed," Dr Vanchinathan added. Mineral (or inorganic) sunscreens contain filters such as zinc oxide and titanium dioxide, while chemical (or organic) sunscreens contain filters such as avobenzone and octocrylene. Unlike inorganic sunscreens, organic sunscreens are designed to absorb into the skin completely.¹⁰

Patients may express concerns about the systemic absorption of chemical filters and potential associated risks, including endocrine-disrupting effects observed in some studies.^4,11,12 Although findings on this topic have been mixed overall, experts have noted the need for further study and industry testing of these potential risks linked to chemical sunscreens.^4,12,13 

"Both chemical and mineral options are safe, and patient preferences can guide their choice of which kind they want to use," Dr Kannan said. "Mineral filters remain an alternative for patient who prefer a non-absorbing option."

Dr Grossberg reiterated that the available evidence overwhelmingly shows that UV radiation from the sun is a proven carcinogen. "UV radiation is classified by the World Health Organization as a Group 1 carcinogen — in the same category as tobacco — and it is directly implicated in the development of skin cancers in humans," she said.⁹ "In contrast, concerns about sunscreen or certain sunscreen ingredients are largely theoretical and unproven, and the benefits of sunscreen in preventing melanoma and other skin cancers far outweigh theoretical risks in studies that have shown no harm of sunscreens in humans." 

"Sunscreen blocks all vitamin D production." 

"Real-world studies show that typical sunscreen use does not cause vitamin D deficiency," Dr Kannan commented.

Findings of a cross-sectional study published in 2022 showed negative correlations between sun exposure and self-reported vitamin D deficiency among US adults. No association was found between sunscreen use and vitamin D deficiency, similar to results observed in previous studies.¹⁴

"Brief incidental sun exposure, oral vitamin D supplementation, and certain foods maintain adequate 25-OH vitamin D levels without sacrificing skin integrity," Dr Kannan explained. Food sources of vitamin D include egg yolks, fatty fish, and red meat, as well as fortified foods and beverages including cereals and milk.¹⁴

"Natural oils like coconut oil or beef tallow provide adequate sun protection."

"The idea that natural oils, such as coconut oil, offer meaningful protection from the sun's harmful UV rays is simply false," Dr Grossberg stated. "While some natural oils may have SPF ranging from 2 to 8, this is well below the protection needed to prevent skin cancer or sun damage."¹⁵

These oils also "lack UVA coverage, degrade quickly, and fail water-resistance standards," Dr Kannan added. "Relying on these oils for sun protection invites cumulative DNA damage, skin cancers, and photoaging down the road."

"Coconut oil and similar substances cannot replace FDA-approved sunscreens," Dr Vanchinathan said.

"Developing a solar callus can protect the skin from UV damage." 

"The idea that you can build up a natural resistance to UV exposure over time is another that has become popular recently," according to Dr Grossberg. "However, a solar callus — or skin hardening, as it's sometimes called — is really just another term for a getting a tan and does not meaningfully increase resistance to or provide protection from solar radiation."

"While melanin provides a minimal degree of additional protection, tanning reflects DNA damage and does not prevent further UV harm," Dr Vanchinathan said.

"A tan does not provide protection against the sun, and there is no such thing as safe tan," Dr Kannan stated. "It's better to use clothing and sunscreen for sun protection."

Dr Grossberg emphasized the need for clinicians to correct misconceptions about sun protection while acknowledging patient concerns and remaining non-judgmental. "Often, when our patients or their family members learn they may be putting themselves or their children at increased risk for skin cancer, they are open to more discussion on how to mitigate these risks," she said. "Taking the time to explain the safety data behind our sunscreen recommendations goes a long way."

To address sun protection myths in the clinic, providers should "invite questions, acknowledge concerns, then share concise data and provide take-home infographics in plain language," Dr Kannan recommended.⁹ "Partner with colleagues who specialize in primary care, pediatrics, and obstetrics and gynecology to ensure consistent messaging across specialties."

To counter sun protection myths on social media, "Clinicians engaging credible voices online and also creating their own dynamic, evidence-based social media content can help counteract misinformation," Dr Vanchinathan explained.

For dermatologists creating their own content, "Produce short, engaging reels debunking single myths (for example, beef tallow ≠ sunscreen), use trending audio for reach, and link to peer-reviewed summaries," Dr Kannan advised. She further suggested working with social platforms to "flag demonstrably false health claims and boost evidence-based content."

Public Health and Community Efforts

Along with efforts to correct sun protection myths in the clinic, ongoing public health measures and community-based approaches are needed.¹⁶

"Public health campaigns that are modernized and accessible can help counter this misinformation trend," Dr Grossberg said. "These may include leveraging social media with dermatologist-backed content, promoting sun safety in schools, as well as regulating marketing that falsely promotes some of these unsafe or less effective products." She also cited the need to encourage companies to share product safety data transparently.

Dr Kannan suggested the implementation of national UV-safety campaigns modeled on anti-tobacco efforts, featuring real melanoma survivors and clear calls to action. Additional recommendations include the integration of photoprotection education into school curricula, engagement in community outreach by offering brief sun-safety sessions at local schools and community centers, and provision of free skin cancer screenings at workplaces, beaches, and sporting events to normalize sunscreen as routine health care.

Dr Kannan also noted that sunscreen is 1 pillar of sun protection and that "UV protective clothing, wide-brimmed hats, midday shade, and behavior change can multiply protection and lessen dependence on any single modality."¹⁷  

References:

 

1. Herman C, Harb N, Ghazarian M, Belzile E, Morena N, Meguerditchian AN. BIO25-022: why don't they want to wear sunscreen? quantifying anti-sunscreen messaging on TikTok. J Natl Compr Canc Netw. 2025;23(3.5):BIO25-022. doi:10.6004/jnccn.2024.7105
2. Nikookam Y, Potluru A, Guckian J. Comment on 'a cross-sectional analysis of TikTok content relating to sunscreen conspiracy theories and correlation with published evidence on sunscreen risks': debunking sunscreen myths and trends – lessons for dermatology educators. Clin Exp Dermatol. 2025;50(5):1025–1027. doi:10.1093/ced/llae492
3. Silva HM. Misinformation about sunscreens on Brazilian social networks: a risk to public health. Trends in Medical Research. 2024;19(1):285-292. doi.org:10.3923/tmr.2024.285.292
4. Sander M, Sander M, Burbidge T, Beecker J. The efficacy and safety of sunscreen use for the prevention of skin cancer. CMAJ. 2020;192(50):E1802-E1808. doi:10.1503/cmaj.201085
5. Dale Wilson B, Moon S, Armstrong F. Comprehensive review of ultraviolet radiation and the current status on sunscreens. J Clin Aesthet Dermatol. 2012;5(9):18-23. Accessed August 9, 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC3460660/pdf/jcad_5_9_18.pdf
6. American Academy of Dermatology. What to wear to protect your skin from the sun. Accessed August 9, 2025. https://www.aad.org/public/everyday-care/sun-protection/shade-clothing-sunscreen/what-to-wear-protect-skin-from-sun
7. American Cancer Society. Spend time outside and stay sun-safe. Published March 7, 2025. Accessed August 9, 2025. https://www.cancer.org/cancer/latest-news/stay-sun-safe-this-summer.html
8. Brar G, Dhaliwal A, Brar AS, et al. A comprehensive review of the role of UV radiation in photoaging processes between different types of skin. Cureus. 2025;17(3):e81109. doi:10.7759/cureus.81109
9. The World Medical Association. WMA statement on solar radiation and photoprotection. Published October 26, 2021. Accessed August 9, 2025. https://www.wma.net/policies-post/wma-statement-on-solar-radiation-and-photoprotection/
10. Raymond-Lezman JR, Riskin SI. Sunscreen safety and efficacy for the prevention of cutaneous neoplasm. Cureus. 2024;16(3):e56369. doi:10.7759/cureus.56369
11. Matta MK, Florian J, Zusterzeel R, et al. Effect of sunscreen application on plasma concentration of sunscreen active ingredients: a randomized clinical trial. JAMA. 2020;323(3):256-267. doi:10.1001/jama.2019.20747
12. Jaskulak M, Cinkusz M, Franchuk K, Zorena K. Endocrine and reproductive health considerations of sunscreen UV filters: insights from a comprehensive review 2014-2024. Curr Environ Health Rep. 2025;12(1):28. doi:10.1007/s40572-025-00492-9
13. US Food and Drug Administration. FDA In Brief: FDA announces results from second sunscreen absorption study. Published January 20, 2020. Accessed August 9, 2025. https://www.wma.net/policies-post/wma-statement-on-solar-radiation-and-photoprotection/
14. Andrade JM, Grandoff PG, Schneider ST. Vitamin D intake and factors associated with self-reported vitamin D deficiency among US adults: a 2021 cross-sectional study. Front Nutr. 2022;9:899300. doi:10.3389/fnut.2022.899300
15. Arkhipenko Z, Shah SC, Yi RC, Feldman SR. A review on homemade sunscreen. Journal of Integrative Dermatology. Published online April 7, 2025. Accessed August 9, 2025.
16. Love B, Ghosh C, Oestman K, et al. Understanding the impact of community-based sun safety interventions on a college campus in Texas. J Am Coll Health. 2024:1-8. doi:10.1080/07448481.2024.2367989
17. American Academy of Dermatology. Sunscreen FAQs. Last update February 11, 2025. Accessed August 9, 2025. https://www.aad.org/media/stats-sunscreen

Tori Rodriguez, MA, LPC, AHC

FDA Alert Highlights DPD Deficiency Warnings for 5-FU, Capecitabine - Dermatology Advisor

https://www.dermatologyadvisor.com/news/fda-alert-highlights-dpd-deficiency-warnings-for-5-fu-capecitabine/?utm_source=eloqua&utm_medium=email&utm_campaign=NWLTR_DER_UPDT_SS-LIC-LAS-PP-10041_SL_021126_AF&hmemail=arj%2Fdu47fH0tIG%2BOxiMnyzIZDo7e%2Fi8h&sha256email=818ca2c110aeb8c0905b76eae9c8cf13eeedcf69cfe6587b8903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True

FDA Alert Highlights DPD Deficiency Warnings for 5-FU, Capecitabine

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February 10, 2026

The Food and Drug Administration (FDA) has issued a safety alert to increase awareness of previous updates to the prescribing label for capecitabine (Xeloda^®) and fluorouracil (5-FU) products related to risks associated with dihydropyrimidine dehydrogenase (DPD) deficiency.

Capecitabine and 5-FU are both nucleoside metabolic inhibitors approved for various cancers. Capecitabine is indicated for colorectal, breast, gastric, esophageal, gastroesophageal junction, and pancreatic cancers, while 5-FU is indicated intravenously for adenocarcinomas of the colon, rectum, breast, stomach, and pancreas, as well as topically for multiple actinic or solar keratoses and superficial basal cell carcinoma. 

According to the safety alert, patients with specific homozygous or compound heterozygous variants in the DYPD gene are at a greater risk for toxicity. These variants lead to a deficiency of the DPD enzyme, which is responsible for breaking down more than 80% of 5-FU. As a result, exposure to capecitabine or 5-FU in these patients can lead to acute early-onset toxicity as well as other serious adverse reactions, such as mucositis, diarrhea, neutropenia, and neurotoxicity.

In response, the FDA approved various safety revisions to the capecitabine and 5-FU product labels. Specifically, a new boxed warning was added to note the risk of serious adverse reactions or death in patients with complete DPD deficiency. The warning further advises that DPYD testing be performed prior to starting capecitabine or 5-FU, unless immediate treatment is necessary. If testing shows complete DPD deficiency, treatment with these nucleoside metabolic inhibitor therapies should be avoided entirely.

The prescribing information was also updated to include a new subsection in the Dosage and Administration and Warnings and Precautions sections to reiterate the need for evaluation and testing for DPD deficiency before starting capecitabine or 5-FU. Moreover, the new labeling highlights the need for caution in those with partial DPD deficiency, emphasizing that dosages for these patients should be individualized and modified based on tolerability and intent of treatment.

The FDA recommends that all health care providers be aware of the risks of DPD deficiency and test for DPYD genetic variants prior to starting treatment, except in cases where immediate treatment is necessary. Additionally, providers should inform patients prior to treatment with capecitabine or 5-FU of the potential toxicities associated with DPD deficiency. 

Adverse reactions associated with the use of capecitabine or 5-FU should be reported to the FDA's MedWatch program.

This article originally appeared on MPR

US Food and Drug Administration. Safety labeling update for capecitabine and fluorouracil (5-FU) on risks associated with dihydropyrimidine dehydrogenase (DPD) deficiency. February 5, 2026. https://www.fda.gov/drugs/resources-information-approved-drugs/safety-labeling-update-capecitabine-and-fluorouracil-5-fu-risks-associated-dihydropyrimidine. 

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Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

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Cx vs Radiotx en KC

Comparison of Surgery vs Radiation Therapy for Non-Melanoma Skin Cancers

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Haley O'Meara, PA-C 

January 30, 2026

Non-melanoma skin cancer (NMSC), also referred to as keratinocyte carcinoma, primarily consists of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).¹ Combined, BCC and SCC make up nearly 95% of skin malignancies and are the most commonly diagnosed cancers in humans.^2,3 The primary risk factor for developing NMSC is ultraviolet radiation from the sun or artificial sources, which cause DNA alterations, as well as production of reactive oxygen species and a reduction in cell-mediated immune responses, leading to cellular damage.^4-7

The prognosis for NMSC is favorable when it is discovered early, although this varies by subtype based on the subtype's behavior and potential to metastasize.²  BCC is less prone to metastasize but can be locally aggressive and invade nearby structures, whereas SCC has a higher tendency to be aggressive and spread to regional lymph nodes.⁸ Untreated NMSC lesions can lead to functional impairment, pain, changes in appearance, and even death, making timely treatment important.

Surgery is the traditionally preferred treatment for most cases of NMSC, with Mohs micrographic surgery (MMS) being the gold standard for NMSC lesions that are high risk, recurrent, or located in anatomically sensitive areas.^1,9 A non-surgical alternative known as image-guided superficial radiation therapy (IG-SRT) has demonstrated remarkable efficacy in the treatment of NMSC lesions and is emerging as a prominent treatment modality.^10,11

Mohs Surgery: The Gold Standard

MMS, developed in the 1930s by Dr Frederic Mohs, serves as the gold standard approach for treating select NMSC lesions.^8,9  As noted, MMS is the standard of care for NMSC lesions categorized as high risk, recurrent, or located in anatomically sensitive areas.^1,9 The MMS technique focuses on precision and tissue preservation.^8,12 The development of this procedure marked a significant advancement in the management of NMSC, as it preserves both appearance and function compared with the standard surgical technique.

Efficacy

MMS has proven to be highly efficacious based on extensive research. A comprehensive 5-year study on the outcomes of MMS showed a 99% cure rate for the treatment of primary BCCs and a 92% to 99% cure rate for the treatment of SCCs.¹³ MMS also has demonstrated a higher cure rate than standard excision for the management of high-risk NMSC lesions.⁸ The thorough approach taken during MMS reduces the likelihood of incomplete removal of the skin cancer roots.¹²

Safety and Cosmetic Outcomes

Overall, patients tolerate MMS well and express high satisfaction regarding cosmetic results. The minimally invasive technique used in MMS focuses on tissue preservation. The procedure is performed under local anesthesia and begins with the removal of a thin, 1- to 2-mm margin of tissue.^8,12,13 The specimen is frozen, sectioned into thin slices, stained, and placed onto slides to evaluate for any remaining cancer cells under a microscope.^8,13 If positive margins remain, the patient is prepped for a second stage and the procedure is repeated until margins are clear of residual cancer cells.¹³ Once complete clearance of margins is achieved, the Mohs surgeon typically closes the surgical site the same day with a complex linear closure, skin flap, or graft depending on the skin defect.¹² After closure, the patient typically is given aftercare instructions and a follow up visit is scheduled for suture removal, if necessary.  In contrast, a standard excision involves the removal of 4- to 6-mm margins down to the mid-subcutaneous adipose tissue.^1,8

Read More: Squamous Cell Carcinoma Stages (in situ, 1-4, metastatic)

It is also important that patients receive clear instructions on wound care to reduce the risk for complications and promote optimal healing. Although most patients experience pleasing cosmetic results with MMS, some can have distress related to scarring, bandaging, or sutures postprocedure.¹⁴ Complications that arise after MMS include bleeding, infection, nerve damage, and reopening of the wound.¹¹ To reduce the risk for complications, some patients are prescribed prophylactic antibiotics or asked to temporarily discontinue their anticoagulant medication for a period of time before the procedure.¹²

Patients with a pacemaker or implantable cardioverter defibrillator may need to turn off their cardiac device, if possible, or have the Mohs surgeon use a disposable electrocautery device to eliminate concerns related to the use of standard electrocautery.¹²

Patient Eligibility 

Determining patient eligibility for MMS is a crucial step in ensuring procedure appropriateness and success. The American Academy of Dermatology (AAD) recommends MMS for all high-risk NMSCs.⁸ High-risk NMSCs may include tumors that are larger than 2 cm, invasive histologic subtypes, sites with high recurrence rates, or sites in anatomical locations where tissue preservation is required.^1,13 MMS is not recommended for patients with medical comorbidities that reduce overall general health or for patients who have abnormal bleeding tendencies.¹⁰

IG-SRT: A Non-Invasive Alternative

IG-SRT was approved by the Food and Drug Administration in 2015. IG-SRT was developed to enhance the effectiveness of superficial radiation therapy (SRT),¹¹ which previously was used by dermatologists to treat NMSC but was replaced by MMS because of the higher cure rates seen with the surgery.¹⁵ IG-SRT uses a high-resolution dermal ultrasound and Doppler features to visualize the depth, width, and overall structure of skin tumors before, during, and after treatment.¹⁵IG-SRT is a precise procedure administered by a board-certified radiation therapist.^11,16

"Studies of IG-SRT report a greater than 99% local cure rate for early-stage NMSC lesions. MMS has a 5-year local control rate of 99% for BCC lesions and 92% to 99% for SCC lesions."

The technique begins with ultrasound visualization of the exact dimensions of the skin tumor.^3,11 Because the ultrasound imaging allows the tumor to be visualized prior to, during, and after treatment, the provider can adjust radiation dosages, if needed, and confirm lesion response to treatment.¹⁵ A 22-MHz high-resolution dermal ultrasound is used, which allows for visualization of skin depths up to 6 mm.¹⁰ The energies of penetration range from 50 to 100 kV and are calculated by using the tumor dimensions, as well as percentage depth dose tables provided by the ultrasound device manufacturer.^10,16 Treatment typically lasts 15 minutes and occurs 3 to 5 times per week for 4 to 7 weeks.¹¹

Efficacy

The use of image-guided ultrasound has made IG-SRT a treatment that is superior to SRT and that demonstrates cure rates that are comparable to those of MMS.¹⁵ In a recent study evaluating IG-SRT for histologically proven NMSC lesions, 2897 out of 2917 lesions showed no signs of residual tumor after treatment, resulting in a 99.3% local control rate.¹⁵ Another study examined 1899 NMSC lesions undergoing IG-SRT for 7.5 weeks showed a local control rate of 99.7%.¹⁶ Data from these studies showing the high local cute rate of over 99%, which supports IG-SRT as a highly effective treatment modality for managing NMSCs.¹⁶

Safety and Cosmetic Outcomes

IG-SRT is a well-tolerated, safe procedure that yields favorable cosmetic results.¹⁰ This procedure uses precise, low-penetration kilovoltage (kV) to target superficial skin lesions, avoiding damage to healthy tissue or deeper structures.¹⁶ IG-SRT's noninvasive technique helps preserve tissue in cosmetically sensitive areas, resulting in exceptional cosmetic outcomes.¹⁵

The procedure has demonstrated a mild side effect profile. Most side effects typically are self-resolving and last for 2 to 6 weeks following treatment.^11,16 Common side effects include hyperpigmentation, desquamation, erythema, and dryness, which can be controlled with over-the-counter cream or ointment.^10,11,16

Patient Eligibility

IG-SRT is an attractive treatment option for patients with superficial NMSCs, as well as patients who refuse surgery or are not surgical candidates. This procedure is recommended by the AAD for patients with early-stage NMSC who do not qualify for surgery.¹⁶ It also can be beneficial for patients with NMSC lesions located in cosmetically sensitive areas.¹⁵ However, not all patients are candidates for IG-SRT because of various contraindications. These include lesions that invade bone or muscle or have a depth greater than 6 mm, a past history of radiation therapy to the same site, connective tissue disease, rheumatologic disease, or current use of chemotherapy agents that increase sensitivity to radiation.¹⁵ Both patient eligibility and contraindications should be reviewed before offering IG-SRT as an option.

Comparative Analysis

MMS and IG-SRT both demonstrate high local cure rates in the management of NMSC, with IG-SRT showing a greater than 99% local cure rate for early-stage NMSC lesions,^15,16 and MMS demonstrating a 5-year local control rate of 99% for BCC lesions and 92% to 99% for SCC lesions.¹⁰ As a noninvasive approach, IG-SRT is a valuable treatment modality, especially when surgery is not preferred or is contraindicated.  MMS has proven to be highly effective in this setting and currently is the gold standard treatment for most NMSC lesions. Although both procedures offer exceptional local cure rates, factors such as patient preference, patient eligibility for the procedure, and lesion characteristics should be considered when choosing a treatment method to ensure safe, favorable outcomes.

MMS with IG-SRT each have advantages and disadvantages related to safety and cosmetic outcomes. MMS is notable for preserving tissue and taking minimal margins.¹ Since this is a surgical procedure, there is a risk for scarring, bleeding, and infection.¹¹ Special consideration must be given to patients with cardiac devices, as well as those who require prophylactic antibiotics or are on certain medications, such as anticoagulants.¹² However, the majority of complications can be taken care of in-office, and patients typically are happy with the cosmetic results following surgery.^12,14 

IG-SRT has favorable results without the need for surgical intervention. It avoids complications such as scarring, infection, and bleeding that can be seen with MMS.^1,15 This is especially important in patients who have skin that is prone to scarring or keloids.¹⁶ IG-SRT also offers advantages over MMS by preserving tissue in lesions in cosmetically challenging areas, such as the scalp, where closure is difficult, or lower legs, which heal more slowly because of poor vascularization, posing a higher risk for infection.¹⁵ It is also important to note that IG-SRT does not require local anesthesia, discontinuation of medications, or prophylactic antibiotics.¹¹

MMS is typically completed during one office visit and takes about 2 to 4 hours depending on the number of stages needed to reach tumor clearance.¹¹ A 1-day procedure is especially important to consider for patients who live far from the office, have trouble commuting to it, or have limited time off work. 

Unlike MMS, IG-SRT has the capability to treat up to 4 lesions at once.^11,16 This provides a significant advantage for patients who have multiple NMSC lesions that need to be treated. IG-SRT also has a shorter office visit time of about 15 minutes but requires 3 to 5 treatments a week over the course of 4 to 7 weeks.¹¹ While the shorter office visits sound appealing, the treatment course requires commitment from patients for multiple visits to ensure that treatment is effective.

Although MMS is the gold standard for NMSC treatment, surgery may be contraindicated in patients with certain medical conditions, such as chronic edema, bleeding abnormalities, or cardiac conditions, and IG-SRT could be used as an alternative in such cases.^11,16 In addition, a patient may decline MMS due to personal preference and opt to receive IG-SRT.

IG-SRT does have limitations and cannot be used in certain scenarios. For example, lesions that are larger than 2 cm or have previously received radiation therapy are contraindicated for IG-SRT; in such cases, MMS may be a better option.¹⁵Eligibility and contraindications for MMS and IG-SRT require careful consideration on a case-by-case basis before choosing an appropriate procedure for each patient. 

Conclusion

When comparing MMS to IG-SRT, preservation of function and cosmesis, along with patient preference and tumor characteristics should be considered by both the patient and provider. Both procedures are considered safe and well-tolerated, with high patient satisfaction rates. When formulating a treatment plan for a patient with NMSC, the efficacy, safety, and cosmetic outcomes, procedure details, and patient eligibility for each procedure should be considered to ensure optimal outcomes.

This article originally appeared on Clinical Advisor

References:

1. Firnhaber JM. Basal cell and cutaneous squamous cell carcinomas: diagnosis and treatment. Am Fam Physician. 2020;102(6):339-346.
2. Didona D, Paolino G, Bottoni U, Cantisani C. Non melanoma skin cancer pathogenesis overview. Biomedicines. 2018;6(1):6. doi:10.3390/biomedicines6010006
3. Catalano O, Roldán FA, Varelli C, Bard R, Corvino A, Wortsman X. Skin cancer: findings and role of high-resolution ultrasoundJ Ultrasound. 2019;22(4):423-431. doi:10.1007/s40477-019-00379-0

4. Paulitschke V, Gerner C, Hofstätter E, et al. Proteome profiling of keratinocytes transforming to malignancy. 2015;36(4):564-576. doi: 10.1002/elps.201400309
5. Ouhtit A, Muller HK, Gorny A, Ananthaswamy HN. UVB-induced experimental carcinogenesis: dysregulation of apoptosis and p53 signalling pathway. Redox Rep.2000;5(2-3):128-129. doi: 10.1179/135100000101535447
6. López-Camarillo C, Ocampo EA, Casamichana ML, Pérez-Plasencia C, Álvarez-Sánchez E, Marchat LA. Protein kinases and transcription factors activation in response to UV-radiation of skin: implications for carcinogenesis. Int J Mol Sci.2012;13(1):142-172. doi: 10.3390/ijms13010142
7. Rittié L, Fisher GJ. UV-light-induced signal cascades and skin aging. Ageing Res Rev.2002;1(4):705-720. doi: 10.1016/s1568-1637(02)00024-7
8. Badash I, Shauly O, Lui CG, Gould DJ, Patel KM. Nonmelanoma facial skin cancer: a review of diagnostic strategies, surgical treatment, and reconstructive techniques. Clin Med Insights Ear Nose Throat. 2019;12:1179550619865278. doi:10.1177/1179550619865278

9. Dika E, Scarfì F, Ferracin M, et al. Basal cell carcinoma: a comprehensive review. Int J Mol Sci. 2020;21(15):5572. Published 2020;21(15):5572. doi:10.3390/ijms21155572
10. Yu L, Oh C, Shea CR. The treatment of non-melanoma skin cancer with image-guided superficial radiation therapy: an analysis of 2917 invasive and in situ keratinocytic carcinoma lesions. Oncol Ther. 2021;9(1):153-166. doi:10.1007/s40487-021-00138-4

11. McClure EM, Sedor G, Jin Y, Kattan MW. Image-guided superficial radiation therapy has superior 2-year recurrence probability to Mohs micrographic surgery. Clin Transl Radiat Oncol. 2023;43:100678. doi:10.1016/j.ctro.2023.100678
12. Bittner GC, Cerci FB, Kubo EM, Tolkachjov SN. Mohs micrographic surgery: a review of indications, technique, outcomes, and considerations. An Bras Dermatol. 2021;96(3):263-277. doi:10.1016/j.abd.2020.10.004

13. Chen ELA, Srivastava D, Nijhawan RI. Mohs micrographic surgery: development, technique, and applications in cutaneous malignancies. Semin Plast Surg. 2018;32(2):60-68. doi:10.1055/s-0038-1642057

14. Vaidya TS, Mori S, Dusza SW, Rossi AM, Nehal KS, Lee EH. Appearance-related psychosocial distress following facial skin cancer surgery using the FACE-Q Skin Cancer. Arch Dermatol Res. 2019;311(9):691-696. doi:10.1007/s00403-019-01957-2
15. Yu L, Moloney M, Zheng S, Rogers J. High resolution dermal ultrasound (US) combined with superficial radiation therapy (SRT) versus non-image guided SRT or external beam radiotherapy (XRT) in early-stage epithelial cancer: a comparison of studies. BMC Cancer. 2023;23(1):98. doi:10.1186/s12885-023-10577-z
16. Tran A, Moloney M, Kaczmarski P, et al. Analysis of image-guided superficial radiation therapy (IGSRT) on the treatment of early-stage non-melanoma skin cancer (NMSC) in the outpatient dermatology setting. J Cancer Res Clin Oncol. 2023;149(9):6283-6291. doi:10.1007/s00432-023-04597-2

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Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

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